Granuloma annulare encompasses an uncommon benign group of granulomatous diseases that include localized, disseminated (generalized), subcutaneous, and perforating types. Approximately 10% to 15% of patients have disseminated granuloma annulare (DGA, also referred to as GGA), which occurs primarily in adults and is characterized by multiple discrete or confluent papules with either an annular or nonannular configuration.1-3 DGA occurs predominantly on the trunk and proximal extremities, and patients with DGA may present with hundreds of lesions. In approximately one third of cases, patients report symptoms of pruritus or burning sensations.2 Histologically, DGA typically is characterized by areas of collagen alteration and elastic fiber degeneration in the middle and upper dermis surrounded by palisading inflammatory cells; the epidermis appears normal.3-6 The inflammatory infiltrates in DGA are primarily composed of a mixture of histiocytes (macrophages) and lymphocytes.4 
Although numerous theories have been proposed to explain the cause of granuloma annulare, the pathogenesis of this cutaneous disease remains unclear. Hypotheses include vasculitis, trauma-induced primary necrobiosis, monocytic release of lysosomal enzymes causing necrobiotic degeneration, and lymphocyte-mediated delayed hypersensitivity reaction (reviewed in Smith et al, 1997).7 Several lines of evidence suggest a role for T-cell-mediated processes in the pathogenesis of granuloma annulare. Activated T lymphocytes, predominantly of the helper T (Th) cell phenotype, have been identified as the dominant lymphocyte in granuloma annulare infiltrates.8-11 Activated Th cells secrete various proinflammatory cytokines, including interleukins, interferon-γ (IFN-γ), and tumor necrosis factor-α (TNF-α),12 all of which have been detected in granuloma annulare lesions.11,13 It has been suggested that initial infiltration of a minor, antigen-specific T-cell population (driven by the presence of unknown skin-specific antigens) is followed by recruitment of a large number of nonspecific T cells by means of nonspecific inflammatory cytokine and chemokine production.14 
Granuloma annulare lesions typically persist for 3 to 4 years, and following spontaneous resolution of lesions, relapse may occur.3 There is no standard treatment regimen or approach employed in the management of patients with granuloma annulare. Furthermore, the response to long-term conventional treatment is generally poor, and in many cases, the risk of serious toxicity does not outweigh the benefits of treatment.2 However, as DGA can be cosmetically disfiguring and as the lesions can persist indefinitely15, many different therapies have been tried with varied success, including cyclosporine,16,17 isotretinoin,18-20 etretinate,21 topical and systemic corticosteroids,22,23 fumaric acid esters,24 psoralens plus ultraviolet A (PUVA),25,26 potassium iodide,27,28 pentoxifylline,29 topical vitamin E,30 hydroxychloroquine,31 dapsone,19,32,33 niacinamide,34 low-dose chlorambucil,35,36 clofazimine,37 and a 5-lipoxygenase inhibitor plus vitamin E.38 Many of these treatments are associated with potentially harmful side effects and require clinical and laboratory monitoring; due to their cumulative toxicity, many of these treatments cannot be administered chronically.
Thus, there is a need for a better method of treating granuloma annulare. The present invention satisfies this need and provides other benefits that will be apparent from the disclosure below.